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We propose a physical theory underlying the temporal evolution of competing virus variants that relies on the existence of (quasi) fixed points capturing the large time scale invariance of the dynamics. To motivate our result we first modify the time-honoured compartmental models of the SIR type to account for the existence of competing variants and then show how their evolution can be naturally re-phrased in terms of flow equations ending at quasi fixed points. As the natural next step we employ (near) scale invariance to organise the time evolution of the competing variants within the effective description of the epidemic Renormalization Group framework. We test the resulting theory against the time evolution of COVID-19 virus variants that validate the theory empirically.
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To better predict the dynamics of spread of COVID-19 epidemics, it is important not only to investigate the network of local and long-range contagious contacts, but also to understand the temporal dynamics of infectiousness and detectable symptoms. Here we present a model of infection spread in a well-mixed group of individuals, which usually corresponds to a node in large-scale epidemiological networks. The model uses delay equations that take into account the duration of infection and is based on experimentally-derived time courses of viral load, virus shedding, severity and detectability of symptoms. We show that because of an early onset of infectiousness, which is reported to be synchronous or even precede the onset of detectable symptoms, the tracing and immediate testing of everyone who came in contact with the detected infected individual reduces the spread of epidemics, hospital load, and fatality rate. We hope that this more precise node dynamics could be incorporated into complex large-scale epidemiological models to improve the accuracy and credibility of predictions.
Several analytical models have been used in this work to describe the evolution of death cases arising from coronavirus (COVID-19). The Death or `D model is a simplified version of the SIR (susceptible-infected-recovered) model, which assumes no recovery over time, and allows for the transmission-dynamics equations to be solved analytically. The D-model can be extended to describe various focuses of infection, which may account for the original pandemic (D1), the lockdown (D2) and other effects (Dn). The evolution of the COVID-19 pandemic in several countries (China, Spain, Italy, France, UK, Iran, USA and Germany) shows a similar behavior in concord with the D-model trend, characterized by a rapid increase of death cases followed by a slow decline, which are affected by the earliness and efficiency of the lockdown effect. These results are in agreement with more accurate calculations using the extended SIR model with a parametrized solution and more sophisticated Monte Carlo grid simulations, which predict similar trends and indicate a common evolution of the pandemic with universal parameters.
An epidemiological model is developed for the spread of COVID-19 in South Africa. A variant of the classical compartmental SEIR model, called the SEIQRDP model, is used. As South Africa is still in the early phases of the global COVID-19 pandemic with the confirmed infectious cases not having peaked, the SEIQRDP model is first parameterized on data for Germany, Italy, and South Korea - countries for which the number of infectious cases are well past their peaks. Good fits are achieved with reasonable predictions of where the number of COVID-19 confirmed cases, deaths, and recovered cases will end up and by when. South African data for the period from 23 March to 8 May 2020 is then used to obtain SEIQRDP model parameters. It is found that the model fits the initial disease progression well, but that the long-term predictive capability of the model is rather poor. The South African SEIQRDP model is subsequently recalculated with the basic reproduction number constrained to reported values. The resulting model fits the data well, and long-term predictions appear to be reasonable. The South African SEIQRDP model predicts that the peak in the number of confirmed infectious individuals will occur at the end of October 2020, and that the total number of deaths will range from about 10,000 to 90,000, with a nominal value of about 22,000. All of these predictions are heavily dependent on the disease control measures in place, and the adherence to these measures. These predictions are further shown to be particularly sensitive to parameters used to determine the basic reproduction number. The future aim is to use a feedback control approach together with the South African SEIQRDP model to determine the epidemiological impact of varying lockdown levels proposed by the South African Government.
This paper is concerned with nonlinear modeling and analysis of the COVID-19 pandemic currently ravaging the planet. There are two objectives: to arrive at an appropriate model that captures the collected data faithfully, and to use that as a basis to explore the nonlinear behavior. We use a nonlinear SEIR (Susceptible, Exposed, Infectious & Removed) transmission model with added behavioral and government policy dynamics. We develop a genetic algorithm technique to identify key model parameters employing COVID19 data from South Korea. Stability, bifurcations and dynamic behavior are analyzed. Parametric analysis reveals conditions for sustained epidemic equilibria to occur. This work points to the value of nonlinear dynamic analysis in pandemic modeling and demonstrates the dramatic influence of social and government behavior on disease dynamics.
In this work, we adapt the epidemiological SIR model to study the evolution of the dissemination of COVID-19 in Germany and Brazil (nationally, in the State of Paraiba, and in the City of Campina Grande). We prove the well posedness and the continuous dependence of the model dynamics on its parameters. We also propose a simple probabilistic method for the evolution of the active cases that is instrumental for the automatic estimation of parameters of the epidemiological model. We obtained statistical estimates of the active cases based the probabilistic method and on the confirmed cases data. From this estimated time series we obtained a time-dependent contagion rate, which reflects a lower or higher adherence to social distancing by the involved populations. By also analysing the data on daily deaths, we obtained the daily lethality and recovery rates. We then integrate the equations of motion of the model using these time-dependent parameters. We validate our epidemiological model by fitting the official data of confirmed, recovered, death, and active cases due to the pandemic with the theoretical predictions. We obtained very good fits of the data with this method. The automated procedure developed here could be used for basically any population with a minimum of extra work. Finally, we also propose and validate a forecasting method based on Markov chains for the evolution of the epidemiological data for up to two weeks.
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